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Data from a population-based case-control study of chronic lymphocytic leukemia were analyzed to assess the possible etiologic role of chronic antigenic stimulation. The study, conducted in four geographic areas of the United States (the metropolitan areas surrounding Seattle, Washington, Salt Lake City, Utah, Detroit, Michigan, and Atlanta, Georgia) sought to identify all incident cases (n = 430) among residents diagnosed between July 1, 1977 and December 31, 1981. The responses of these cases to questions about possible sources of antigenic stimulation were compared with the responses of controls selected from the populations of these areas. Little difference between cases and controls was present for a history of most forms of viral and bacterial infection and for a history of allergies or allergy treatment. However, a relation was observed with antecedent syphilis infection (odds ratio (OR) = 5.0, 95% confidence interval (Cl) 2.0-12.9). Associations of smaller magnitude were observed with a history of tuberculosis (OR = 1.9, 95% Cl 1.0-3.7) and of urinary tract infection (OR = 1.4, 95% Cl 1.1-1.9). Overall, however, the authors found little evidence of a relation between chronic antigenic stimulation and the occurrence of chronic lymphocytic leukemia. Nonetheless, because the measure of prior antigenic stimulation was restricted to that obtained through interviews and undoubtedly was an insensitive one, these negative results should not be interpreted as ruling out antigenic stimulation as a possible cause of some cases of chronic lymphocytic leukemia.

The National Cancer Institute diet questionnaire was evaluated for use in a low-income black population. Data were collected from 91 women aged 30-69 years who were hospital outpatients in Atlanta, Georgia, June through August, 1988. Six ethnic and regional foods added to the questionnaire were found to be important contributors to intakes of several nutrients. Although 17 records were identified as containing probable recording or reporting errors, intakes of carotenes, alpha-carotene, beta-carotene, cryptoxanthin, and vitamin E were significantly and positively associated with serum levels of their referent nutrients. Among nonsmokers, correlation coefficients ranged from 0.32 to 0.45, adjusted for age, body mass index, alcohol and calorie intakes, medications and vitamin supplement use, and serum cholesterol and triglycerides. When questionnaires containing identified errors were omitted, correlations ranged from 0.30 to 0.54. There were no correlations between dietary intakes of lycopene and lutein and blood levels (-0.06 to 0.09). Among smokers, diet-serum correlations were reduced (0.00 to 0.32). These correlations are similar to those reported in research on vitamin E and carotenoids in other populations. These results suggest that the questionnaire is as valid for use in this population as it is in other populations.

Glutathione, a tripeptide found in a variety of foods, may function as an anticarcinogen by acting as an antioxidant and by binding with cellular mutagens. The association between dietary glutathione intake and risk of oral and pharyngeal cancer was investigated using data from 1,830 white participants (855 cases and 975 controls) in a population-based case-control study conducted in New Jersey; metropolitan Atlanta, Georgia; Los Angeles County, California; and Santa Clara and San Mateo counties, south of San Francisco-Oakland, California, during 1984-1985. The estimated relative risk of cancer among people with the highest quartile of glutathione intake from all sources was 0.5 (95% confidence interval 0.3-0.7). When analyzed by dietary source, however, glutathione intakes derived from all vegetables and from meat were not related to risk of cancer. Only glutathione derived from fruit and from vegetables commonly consumed raw was associated with reduced oral cancer risk. Relative to the lowest level of combined intake of fruit and of fruit-derived glutathione, risk of cancer decreased slightly with increasing intake of fruit glutathione. This analysis was limited, however, by the small numbers of subjects with extreme combinations of intakes. Further studies are needed to distinguish the potential effect of glutathione from that of fruit and raw vegetables per se or from the influence of other constituents in these foods.

The authors conducted a population-based case-control study of lung cancer in nonsmoking women in five metropolitan areas of the United States between December 1, 1985, and November 30, 1990. In-person interviews were conducted with 412 lung cancer cases and 1,253 population controls, yielding information on history of nonmalignant lung diseases that were diagnosed by a physician. When lung cancer cases were compared with controls, history of any previous lung disease was associated with a significant increased risk of lung cancer (adjusted odds ratio (AOR) = 1.56, 95% confidence interval (CI) 1.2-2.0). Several lung diseases, including asthma, chronic bronchitis, pneumonia, and tuberculosis, were reported more often by lung cancer cases than by controls, and the difference was statistically significant for asthma (AOR = 1.67, 95% CI 1.1-2.5) and chronic bronchitis (AOR = 1.60, 95% CI 1.1-2.4). Since significant increased risks were observed for asthma and tuberculosis diagnosed before age 21 years, it is unlikely that reported prior lung diseases were prediagnostic manifestations of lung cancers. The increased risks associated with previous lung disease were observed for adenocarcinomas and other carcinomas of the lung; the point estimates were generally higher for the latter category. The risks associated with previous lung diseases remained unchanged after adjustment for potential confounders, including environmental tobacco smoke exposure during childhood and adult life and dietary factors.

To evaluate the risk of childhood cancer among infants with serious birth defects, the authors linked records of the population-based registry of the Georgia Center for Cancer Statistics for 1975 to 1988 with records of the population-based Metropolitan Atlanta Congenital Defects Program for 1968 to 1987. During the study period, birth defects were diagnosed in 19,373 infants younger than 1 year of age, and cancer was diagnosed in 400 children younger than 15 years of age. The observed number of children with a defect who developed cancer was compared with the number expected on the basis of the cancer registry rates. Of the 19,373 children with birth defects, 31 developed cancer (standardized incidence ratio (SIR) = 2.2, 95% confidence interval (CI) 1.5-3.2). Two associations were found: of 532 children with Down's syndrome (trisomy 21), three developed acute leukemia (SIR = 50.8, 95% CI 10.5-148.5) while of 746 children with pyloric stenosis, four developed cancer (SIR = 7.5, 95% CI 2.0-19.3). These data show that children with selected birth defects are at increased risk for specific childhood cancers. Such record-linkage can reveal new associations, which can in turn help researchers understand underlying mechanisms common to teratogenesis and carcinogenesis.

A large population-based case-control study was carried out to investigate the association between vasectomy and prostate cancer risk in black and in white men in the United States. Study subjects resided in the geographic areas covered by the population-based cancer registries of the Georgia Center for Cancer Statistics, or the Metropolitan Detroit Cancer Surveillance System, or in 10 counties included in the cancer registry of the New Jersey State Health Department. Cases for this study were men aged 40-79 years identified from pathology and outpatient records at hospitals covered by these registries, newly diagnosed with pathologically confirmed prostate cancer between August 1, 1986, and April 30, 1989. Population controls less than age 65 years were selected at periodic intervals by random digit dialing. Older controls were systematically selected (after a random start) from computerized records of the Health Care Finance Administration. A statistically nonsignificant excess risk (odds ratio (OR) = 1.6, 95% confidence interval (CI) 0.5-4.8) for prostate cancer associated with vasectomy was noted in blacks. Overall, the risk for prostate cancer associated with vasectomy in whites was not elevated (OR = 1.1, 95% CI 0.8-1.7). An increase in risk was found, however, for white men who had had a vasectomy 20 years or more prior to study (OR = 1.7, 95% CI 0.9-3.3) or who had had a vasectomy at less than age 35 years (OR = 2.2, 95% CI 1.0-4.4). For the total study group, the odds ratio associated with men who had a vasectomy 20 or more years prior to study was 1.5 (95% CI 0.8-2.7), and the odds ratio associated with men who had had a vasectomy at less than age 35 years was 2.0 (95% CI 1.0-4.0). Further detailed analysis showed that young age at vasectomy (less than age 35 years) was a more important risk factor than was years since vasectomy.

A population-based case-control study was conducted to examine whether tumor estrogen receptor status differentiated risk factor patterns for breast cancer. From December 1980 to December 1982, 458 women with newly diagnosed breast cancer and 568 control women, aged 20-54 years, from the Atlanta, Georgia, metropolitan area were interviewed. On the basis of tumor estrogen receptor results, cases were classified as receptor-positive or receptor-negative. Intercase analysis showed that age was positively and significantly associated with estrogen receptor-positive breast cancer (p = 0.001); the relative risk for an estrogen receptor-positive as opposed to an estrogen receptor-negative tumor was elevated threefold among women aged 50-54 years compared with those aged less than 35 years. In the case-control analysis, race was the only individual factor that demonstrated a significant difference in the risk for estrogen receptor-positive versus estrogen receptor-negative cancer (p less than 0.05), with blacks being at a 25% excess risk for estrogen receptor-negative cancer compared with whites. Although a history of benign breast disease was a risk factor for both positive and negative tumors, the association was stronger for the estrogen receptor-positive tumors. Postmenopausal women were at a lower risk for both cancer subtypes compared with premenopausal women. Compared with non-users, women who had ever taken oral contraceptives had a 16% decrease in the risk for receptor-positive cancer and a 22% increase in the risk for receptor-negative cancer. These results are consistent with the notion that certain exposure variables may relate to hormonal status, possibly by augmentation or suppression of estrogen receptor activity.